Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Biofilm is a integrated multucellular organism with own cycle of development, cooperative behavior of units forming it, which coordinated by QS-system based on production of signal molecules or autoinductors and ability of bacteria to receive these signals. Presence ofbacteria attached to surface of biomedical devices and formation of bacterial biofilms in the microorganism could lead to chronic inflammation, which characterized by presence of macrophages and lymphocytes in the focus of inflammation as well as proliferation of connective tissue, accumulation of matrix proteins and stimulation ofangiogenesis. Process of biofilm formation associated with activation of QS-system of different agents including potentially dangerous bacteria plays certain role in exacerbation of gastric and duodenal ulcer diseases, Crohn's disease, myocarditis, asthma, diabetes mellitus, cardiovascular and other somatic diseases. Detachment of biofilm could lead to enter ofbac-teria in bloodsream and vascular embolism. Issues related to ability of bacteria of biofilms to modulate immune response and potential for the emerging response to influence the biofilm growth and level of expression of bacterial virulence are discussed. Modem views on mechanisms of interaction of bacteria of exopolysaccharide biofilm with host's immune response factors are reviewed. The most perspective ways to control for biofilm formation and their disruption using newly developing drugs are outlined.
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PMID:[Immunobiological features of bacterial cells of medical biofilms]. 2079 92

Objectives. Ninety-one fetuses with dilated or hypertrophic cardiomyopathy (DCM, HCM) and myocarditis were studied. Results. Group 1 "DCM" included 19 fetuses: 13 with hydrops (FH) and 5 with associated extracardiac anomalies (ECAs) (15.8%). Group 2 "Myocarditis" included twelve fetuses, having 11 with FH. Group 3 "HCM" included sixty fetuses: 26 had associated ECAs, 17 had maternal diabetes, and 17 were "idiopathic"; however, in one case, a metabolic disorder was found postnatally, and 4 had familiarity for HCM. Outcomes. Ten cases opted for termination of pregnancy. Two cases with DCM and 1 with HCM were lost at follow-up. Out of the cases that continued pregnancy, with known follow-up, mortality was 68.75% in Group 1, 63.6% in Group 2, and 31.3% in Group 3 (the majority with severe ECAs). Surviving cases with DCM and myocarditis improved, 2 with HCM worsened, 6 remained stable, and 26 improved or normalized. Conclusions. Our data show more severe prognosis in DCM and myocarditis and forms with severe associated ECAs.
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PMID:Features and outcomes in utero and after birth of fetuses with myocardial disease. 2097 7

Glucocorticoids (GC) are drugs commonly used, by approximately 1% of the total adult population as anti-inflammatory and immunosuppressive therapies for asthma, inflammatory bowel disease, dermatological, ophthalmic, neurological, and rheumatic autoimmune diseases. Supporting evidence exists of GC use in both immune mediated and non-immune mediated heart disease. The molecular mechanisms by which GC induces immune-modulation and direct cardioprotection, are complex and not fully understood. We review herein, the current knowledge of GC use in various immune-mediated or non-immune mediated cardiovascular conditions. GC have been investigated in autoimmune, inflammatory and idiopathic heart diseases such as atrio-ventricular conduction abnormalities, rheumatic fever, myocarditis, dilated cardiomyopathy, Churg-Strauss syndrome, Kawasaki disease and sarcoidosis. GC therapy has been studied in non-autoimmune and non-inflammatory indications such as acute myocardial infarction, angina, postpericardiotomy syndrome and other pericardial diseases, endocarditis and cardiac amyloidosis, as well as in invasive cardiology, coronary interventions, and cardiopulmonary-bypass surgery. Despite GC's role as natural, physiologic regulators of the immune system, cardiovascular adverse outcomes may occur. Some of the well-known side effects of GC therapy involve bone, metabolic, and cardiovascular systems and include osteoporosis, fractures, dyslipidemia, diabetes, obesity, and hypertension.
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PMID:Glucocorticoids and the cardiovascular system: state of the art. 2097 21

This report presents the case of a 47-year-old female patient with fulminant type 1 diabetes mellitus and myocarditis. Following a high fever, nausea, vomiting and diarrhea, diabetic ketoacidosis occurred and she was transferred to the hospital. The plasma glucose level was 63.6 mmol/L and HbA1c was 7.0%. C-peptide was undetectable in her plasma. Blood gas analysis showed a pH of 6.99. Antibodies to glutamic acid decarboxylase nor insulinoma associated antigen-2 were not detected. She was diagnosed to have fulminant type 1 diabetes mellitus. Her electrocardiogram showed diffuse ST-segment elevations on the second day of admission, along with a positive troponin test. However coronary angiography revealed neither occlusion nor stenosis of the cardiac arteries. An endomyocardial biopsy revealed hypertrophic cardiomyocytes with a disarrangement of myofibers and the focal accumulation of mononuclear cells in the stroma, thus suggesting myocarditis or mild myocarditic change. Viruses are an important cause of myocarditis and the preceding flu-like symptoms indicate the association of viral infection with myocarditis in this case. The mechanisms by which fulminant type 1 diabetes mellitus occurs is still uncertain, but the presence of islet injury accompanied by myocardial inflammation in the current case suggested that a viral infection accounted for the onset of this type of diabetes.
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PMID:A case of fulminant type 1 diabetes mellitus accompanied by myocarditis. 2155 59

A case of circulatory collapse due to severe heart failure is reported in a 52-year old male with autoimmune disorders in the form of type-1 diabetes, Graves' disease and total alopecia.Upon admission, the patient had severe heart failure with a cardiac index of 0.9 l/min/m(2), a mixed venous saturation of 29% and left ventricular ejection fraction of 5%. The condition was refractory to treatment with inotropic agents and required mechanical cardiopulmonary support. Endomyocardial biopsies revealed extensive giant cell myocarditis (GCM). Immunosuppressant treatment did not alter the condition and urgent orthotopic heart transplantation was performed.Histopathological examination of the explanted heart confirmed the diagnosis and showed widespread vascular deposition of complement C4d suggesting a pathogenic role for the innate immune system in GCM.At 1-year follow-up the patient was in New York Heart Association (NYHA) class I, had episodes of sustained ventricular tachycardia but showed no evidence of GCM recurrence in endomyocardial biopsies.
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PMID:Fatal giant cell myocarditis in a patient with multiple autoimmune disorders. 2168 15

Encephalomyocarditis virus (EMCV) infection leads to many diseases including encephalitis, myocarditis and diabetes in its natural host, the mouse. In this study, we generated four cDNA clones with a point mutation at position 100 of VP1. The amino acids isoleucine, alanine, serine and proline were substituted with threonine in the four different clones of EMCV strain BJC3 by site-specific mutagenesis, and viable viruses were rescued. Although all mutants and wild-type viruses display different plaque morphologies, they replicate comparably in BHK-21 cells. The pathogenicity of the mutated viruses was systematically analyzed to investigate the importance of this amino acid in the viral pathogenicity and disease phenotype of EMCV infection in mice. The results showed that the isoleucine- (T1100I) and proline-mutated viruses (T1100P) exhibited a reduced mortality, lower cerebral virus loads and alleviated brain damage while the viruses with serine (T1100S) and alanine (T1100A) substitutions displayed similar properties as the wild-type virus. These findings indicate that the amino acid at position 100 of VP1 is important for EMCV in vivo infection, and its mutation alters the pathogenicity of viral infection in mice.
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PMID:Alteration of encephalomyocarditis virus pathogenicity due to a mutation at position 100 of VP1. 2170 14

The scarcity of Trypanosoma cruzi in inflammatory lesions of chronic Chagas disease led early investigators to suggest that tissue damage had an autoimmune nature. In spite of parasite persistence in chronic Chagas disease, several reports indicate that inflammatory tissue damage may not be correlated to the local presence of T. cruzi. A significant number of reports have described autoantibodies and self-reactive T cells, often cross-reactive with T. cruzi antigens, both in patients and in animal models. Evidence for a direct pathogenetic role of autoimmunity was suggested by the development of lesions after immunization with T. cruzi antigens or passive transfer of lymphocytes from infected animals, and the amelioration of chronic myocarditis in animals made tolerant to myocardial antigens. Autoimmune and T. cruzi-specific innate or adaptative responses are not incompatible or mutually exclusive, and it is likely that a combination of both is involved in the pathogenesis of chronic Chagas disease cardiomyopathy. The association between persistent infection and autoimmune diseases-such as multiple sclerosis or diabetes mellitus-suggests that post-infectious autoimmunity may be a frequent finding. Here, we critically review evidence for autoimmune phenomena and their possible pathogenetic role in human Chagas disease and animal models, with a focus on chronic Chagas disease cardiomyopathy.
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PMID:Autoimmunity. 2188 90

The 2009 Pandemic Novel Influenza A [HIN1] resulted in mild disease mostly but severe cases and death were associated with pneumonia, respiratory failure and multi-organ failure. We present a case of severe disease with acute heart failure and arrhythmia due to fulminant myocarditis in a 50- year old obese man with diabetes mellitus.
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PMID:Acute fulminant myocarditis and the 2009 pandemic influenza A virus (H1N1). 2194 31

Clozapine is the best treatment option in several clinical circumstances, including treatment-resistant schizophrenia, non treatment-resistant schizophrenia, suicide risk in schizophrenia spectrum disorders, aggressiveness or violence in psychiatric patients, psychosis in Parkinson's disease, prevention and treatment of tardive dyskinesia. However, clozapine is associated with many serious side effects. Furthermore, monitoring requirements, i.e., frequent blood draws and frequent visits, discourage clozapine use. Therefore, the drug is underused. The only way to avoid the underuse of clozapine is full awareness of its side effects and competence to minimize them. The aim of the paper is reviewing the safety profile of clozapine and the suggested strategies in the management of its side effects, including neutropenia, eosinophilia, seizures, myocarditis, weight gain, diabetes, metabolic syndrome, hypersalivation, fever, constipation, ileus, urinary incontinence, sweating. The neuropsychiatric side effects of clozapine are not discussed in this review.
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PMID:Clozapine safety, 35 years later. 2212 92

Heart failure is a clinical syndrome that results when the heart is unable to provide sufficient blood flow to meet metabolic requirements or accommodate systemic venous return. This common condition affects over 5 million people in the United States at a cost of $10-38 billion per year. Heart failure results from injury to the myocardium from a variety of causes including ischemic heart disease, hypertension, and diabetes. Less common etiologies include cardiomyopathies, valvular disease, myocarditis, infections, systemic toxins, and cardiotoxic drugs. As the heart fails, patients develop symptoms which include dyspnea from pulmonary congestion, and peripheral edema and ascites from impaired venous return. Constitutional symptoms such as nausea, lack of appetite, and fatigue are also common. There are several compensatory mechanisms that occur as the failing heart attempts to maintain adequate function. These include increasing cardiac output via the Frank-Starling mechanism, increasing ventricular volume and wall thickness through ventricular remodeling, and maintaining tissue perfusion with augmented mean arterial pressure through activation of neurohormonal systems. Although initially beneficial in the early stages of heart failure, all of these compensatory mechanisms eventually lead to a vicious cycle of worsening heart failure. Treatment strategies have been developed based upon the understanding of these compensatory mechanisms. Medical therapy includes diuresis, suppression of the overactive neurohormonal systems, and augmentation of contractility. Surgical options include ventricular resynchronization therapy, surgical ventricular remodeling, ventricular assist device implantation, and heart transplantation. Despite significant understanding of the underlying pathophysiological mechanisms in heart failure, this disease causes significant morbidity and carries a 50% 5-year mortality.
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PMID:The pathophysiology of heart failure. 2222 65


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